DiStasi, Matthew R.Mund, Julie A.Bohlen, H. GlennMiller, Steven J.Ingram, David A.Dalsing, Michael C.Unthank, Joseph L.2016-12-192016-12-192015-10DiStasi, M. R., Mund, J. A., Bohlen, H. G., Miller, S. J., Ingram, D. A., Dalsing, M. C., & Unthank, J. L. (2015). Impaired compensation to femoral artery ligation in diet-induced obese mice is primarily mediated via suppression of collateral growth by Nox2 and p47phox. American Journal of Physiology. Heart and Circulatory Physiology, 309(7), H1207-1217. https://doi.org/10.1152/ajpheart.00180.20150363-6135 1522-1539https://hdl.handle.net/1805/11665Novel observations in this report include the demonstration of collateral resistance as the primary limitation of hindlimb perfusion, elevated NADPH oxidase (Nox) expression in peripheral arteries, unimpaired monocyte mobilization and demargination, and reversal of suppressed principle collateral growth by Nox2 ablation/inhibition in a diet-induced obese mouse model of arterial occlusion.en-USPublisher's PolicyNADPH oxidaseNox2arteriogenesiscollateral resistancevascular resistanceArticle